Atrial flutter (AFL) is a supraventricular tachycardia that arises from both substrate and ablation scars.1,2 While typical AFL is treated successfully with cavotricuspid isthmus ablation,3 catheter radiofrequency (RF) ablation results are suboptimal in patients with atypical AFL,4,5 especially when the macroreentrant circuit involves the left atrium. Left AFL ablation usually employs electroanatomic mapping (EAM) systems and entrainment mapping.6 Another possibility is the identification and ablation of the mid-diastolic isthmus.7,8 Nevertheless, the absence of a precise tool to identify the critical isthmus in tachycardia may be one of the reasons for the mixed outcomes using this technique.

Out of 22 patients, nine met the criteria, three of whom were female, with a median age of 75, interquartile range (IQR) 71-76 years. The clinical and arrhythmic characteristics of the nine patients included in this study are presented in Tables 1 and 2.

Six of the nine patients already had a previous pulmonary vein isolation, 2 of them underwent a typical AFL ablation and 1 a mitral AFL ablation (Table 2). Three of the patients had never undergone a catheter ablation procedure. The AFL were perimitral (n=2), roof scar-related (n=2), anterior scar-related (n=1), posterior scar-related (n=1) and right superior pulmonary vein-related (n=1). The median TCL was 254 ms (IQR 220-290). The EAM had a median of 3300 (IQR 2410-3926) points and presented a median of 2 (IQR 1-2) LAT-valleys. The median duration of the primary valleys was 81 ms (IQR 51-84). In the first seven cases, the exact locations for ablation were defined in a standard fashion, whereas in the last two cases the ablation sites were selected taking in to account the cycle length duration and heterogenous scar (two out of the three elements defined in the triad). In both these cases a single RF application suppressed the AFL.

AFL was terminated successfully (100%) in all nine patients during RF application and the arrhythmia termination zone was tagged in a three-dimensional map (Figures 1, 2 and 3). Post-hoc analysis showed that all these areas corresponded to the primary LAT-valley identified in the global histogram analysis. These areas corresponded to small atrial surfaces of 1 to 2 cm2 with heterogenous low-voltage tissue (between 0.05 and 0.3 mV). We also identified a secondary LAT-valley in six of the nine patients (67%). After three months all patients presented sinus rhythm without documented episodes of arrhythmia recurrence.

Figure 1.

Posterior wall-related flutter, with a valley in the local activation time histogram of the global activation (A) which corresponded to an area of delayed conduction on the activation map (B), and a scar surrounding a channel of healthier tissue on the voltage mapping (C); the arrhythmia ended during radiofrequency applications in this area.

LAT: local activation time; RF: radiofrequency.

(0.11MB).

Figure 2.

Flutter around an anterior wall scar and a corresponding local activation time-valley (blue, purple, red and orange bars); radiofrequency application stopped the atrial flutter (blue tag).

AFL: atrial flutter; LAT: local activation time; RF: radiofrequency.

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Figure 3.

Posterior wall-related flutter with a critical isthmus in a heterogeneous low-voltage area, corresponding to the primary valley (magenta bar); the arrhythmia ended after 21 seconds of radiofrequency.

RF: radiofrequency.

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Previous approaches to atypical AFL ablation include heterogeneous catheter ablation techniques.10,11 Most centers combine EAM with entrainment maneuvers to identify critical areas of the reentrant circuit.6,10,12 Some authors also suggest the identification of the mid-diastolic isthmus as a potential ablation target.7,8 We used these conventional techniques for mapping and ablation of these patients. However, the procedures are highly complex and require extensive ablation lesions. The results are suboptimal,6 indicating that such practices are not sufficient to identify the critical isthmus. In our post-hoc analysis, we put forward an electrophysiologic triad to recognize a critical isthmus. This triad identified the critical isthmus in all patients in a limited left atrial surface of 1 to 2 cm2. In fact, deep and large LAT-valleys corresponded to critical isthmi and in these locations the heterogenous low-voltage areas were effective targets for ablation. In a previous report9 with another mapping system (Rhythmia®), there was a correlation between a valley in the global late activation histogram and slow conduction areas. However, one in four of the identified valleys did not correspond to delayed conduction. A possible limitation could be incorrect and insufficient point collection which induces false positive results. In this situation, scar tissue with delayed conduction would not be present. In this study, the triad bypasses this possibility since heterogeneous low-voltage (0.05 to 0.3 mV) and conduction delay (≥10% of TCL included) need to present in the LAT-valley, increasing its specificity and accuracy. Current software tools,6 especially Carto® ripple mapping, only show the global left atrium arrhythmia activation wave front. This novel purposed approach presents an important advantage because it can pinpoint the effective ablation area (1 to 2 cm2). The analysis of the activation maps also identified a secondary LAT-valley in most of the patients. They may be related to additional slow conduction areas which are present in more complex AFL, usually associated with previous iatrogenic scars (e.g. post atrial fibrillation ablation). In this regard, the secondary LAT-valleys are potential therapeutic targets if ablation of the primary valley is not sufficient, especially in patients with more than one reentrant circuit. The electrophysiologic triad is potentially useful for assessing any scar-related tachycardia. In the future, the critical isthmus may be easily targeted in the three-dimensional EAM, to improve and simplify the ablation procedure.

The limitations of this study need to be acknowledged. This was a single-center retrospective study of patients with atypical AFL. Our analysis only assessed patients with effective termination of the arrhythmia, which may have induced survival bias. Also, the small study sample should be taken into consideration in the generalization of our findings. In addition, we lack long-term follow up for relapse of arrhythmia. A randomized study should be performed to clarify whether this tool can improve catheter ablation outcomes.

An electrophysiologic triad identified the critical isthmus in AFL for all patients. Further studies are needed to assess the usefulness of this tool for improving catheter ablation outcomes.

The authors have no conflicts of interest to declare.